2019 Fiscal Year Final Research Report
Molecular basis for the mechanism of ectodermal dysplasia caused by abnormal calcium signaling
| Project/Area Number |
17K11940
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthodontics/Pediatric dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大洞 將嗣 順天堂大学, 医学(系)研究科(研究院), 先任准教授 (40351506)
寺尾 文恵 九州大学, 歯学研究院, 助教 (10510018)
吉崎 恵悟 九州大学, 歯学研究院, 助教 (10507982)
二階堂 まりこ (梅田まりこ) 九州大学, 大学病院, 学術研究員 (40707618)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Keywords | ストア作動性カルシウム流入 / STIM1 / カルシウムイオン / 歯 / エナメル質 / 唾液腺 |
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| Outline of Final Research Achievements |
In this study, we generated and phenotyped epithelium-specific Stim1/2 mutant mice to elucidate the molecular mechanism of store-operated calcium entry (SOCE), involved in the development of ectodermal dysplasia (ED) phenotypes. The results showed that the phenotype of amelogenesis imperfecta (AI) in Stim1/2 mutant mice was almost identical to the human AI, which may be led by the functional changes in the maturation stage of ameloblasts. In addition, Stim1/2 mutant mice had reduced saliva secretion due to altered salivary gland cell function, possibly due to the altered ion channel function resulting in the abnormal intracellular ion concentration such as chloride.
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| Free Research Field |
歯科矯正学
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| Academic Significance and Societal Importance of the Research Achievements |
ストア作動性カルシウム流入(SOCE)の異常は、エナメル芽細胞ならびに唾液腺細胞機能に影響をあたえ、ヒトの外胚葉異形成症の表現型がもたらされることが確認された。これにより、SOCEの上皮細胞における生物学的役割の解明という観点からのみならず、歯の石灰化異常や唾液分泌量低下によるQoL低下防止を目指した歯科医療の基盤的知識の蓄積にも貢献できる、有意義な情報を得ることができたと考えられる。
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